Localized juvenile periodontitis (LJP, Periodontosis) is characterized by a decrease in polymorphonuclear leukocyte (PMN) function. The functional decreases include receptor modulation, chemotaxis, and phagocytosis. Interestingly, all three of these functions depend on the coordinated reorganization of the actin cytoskeleton. Ordered alterations of the actin cytoskeleton, in turn, depend on actin polymerization. We therefore propose to examine the relationship between LJP and the ability of the PMN to polymerize actin. We raise the following question: Is the decreased PMN function observed in LJP mediated by a defect in actin polymerization? To examine this question we will carry out both cross sectional and longitudinal studies. In these studies we will compare the ability of PMNs from LJP and normal controls to polymerize actin upon stimulation. A panel of stimuli will be used. The panel will allow us to answer the posed question, and, in addition, allow us to determine the level of the defect (ie: receptor-ligand interaction; signal transduction; or cytoplasmic response). To quantitate actin alterations, actin first will be specifically labeled with the fluorescent probe NBD phallacidin. Subsequently, actin measurements will be done on a fluorescence activated cell sorter. Covariate analysis for this work will include: chemotaxis, serum antibody titers, and periodontal therapy. The significance of this work is that it will allow us to better understand the relationship between actin polymerization and PMN function, and better define the molecular defect(s) responsible for PMN dysfunction in LJP.